PAT 20A/B Lecture Notes - Lecture 3: Hyperaemia, Arteriole, Mononuclear Phagocyte System
20 Apr 2016
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Document Summary
Vascular response after cell injury, arterioles undergo transient vasoconstriction (by sns) platelets aggregate to seal injured area -> form fibrin-platelet clot -> releases proinflamatorry mediators (histamine) > cause vasodilation -> result hyperemia (increase blood flow in area) > filtration pressure increase -> endothelia cell retraction, increase capillary permeability (movement fluid from capillary into tissue space) Lymphocytes arrive later at injuy site: primary role: related to humoral and cell-mediated immunity, eosinophils and basophils, selective role in inflammation, eosinophils released in large quantities during allergic reaction. Release chemicals control effects of histamine and serotonin. Contain highly caustic chemicals capable of destroying parasites cell surface: histamine and heparin carried by basophils granules released during inflammation. Involved in phagocytosis of allergen-antibody complex: describe chemotaxis. Chemotaxis directional migration of white blood cells along concentration gradient of chemotactic factors (substances that attracts wbs to inflammation site)
